Synopsis
Recognise haematological and neurological vitamin B12 deficiency, determine whether autoimmune gastritis or another cause is responsible, and replace promptly with route and duration matched to reversibility.
- Vitamin B12 deficiency can present with neuropathy, impaired vibration or joint position, ataxia, cognitive or psychiatric change, glossitis or fatigue before anaemia or macrocytosis appears.
- Take pretreatment blood when this causes no harmful delay. Interpret total or active B12 through NICE NG239 thresholds and use methylmalonic acid or homocysteine when the result is indeterminate and symptoms persist.
- Nitrous oxide can produce functional deficiency despite a non-low serum B12. NICE recommends homocysteine or methylmalonic acid testing, but neurological treatment must not wait when suspicion is strong.
- Autoimmune gastritis is the underlying disorder historically linked with pernicious anaemia. Anti-intrinsic-factor antibody supports it, but a negative result does not exclude the diagnosis.
- Use intramuscular hydroxocobalamin when neurological disease is present or malabsorption is likely; high-dose oral replacement can be appropriate for dietary deficiency and selected malabsorption pathways under NICE guidance.
- For suspected malabsorption treated orally, NICE advises at least 1 mg vitamin B12 daily. Check the exact licensed product and adherence rather than relying on low-dose supplements.
- Irreversible autoimmune or anatomical malabsorption generally requires lifelong replacement. Reversible dietary or medicine-related deficiency needs cause correction, planned review and a clear stopping decision.
- Do not treat folate alone until B12 deficiency has been addressed: the blood count may improve while neurological injury continues.
Key red flags
Symmetrical paraesthesia, impaired vibration or proprioception, sensory ataxia, weakness, cognitive change or visual symptoms with risk factors warrants prompt assessment and replacement.
Recreational or repeated medical exposure with rapidly evolving paraesthesia, gait change or weakness suggests functional inactivation even when serum B12 is not low.
Investigation priorities
Classify the initial result within the NICE diagnostic pathway.
Management branches
Neurological symptoms and risk factors suggest vitamin B12 deficiency or nitrous-oxide-mediated functional deficiency.
- Take B12 and functional-marker samples if immediately available, document a full neurological examination and exposure history, and stop nitrous oxide, but do not delay replacement for results.
- Preferred UK treatment is hydroxocobalamin 1 mg intramuscularly on alternate days until no further improvement, followed by the maintenance schedule when the cause is irreversible.
- Escalate rapid progression, weakness, gait or sphincter disturbance, visual change, severe psychiatric symptoms or diagnostic uncertainty to neurology and haematology while continuing supported treatment.
Key medicines
Hydroxocobalamin with neurological involvementGive 1 mg intramuscularly on alternate days until no further improvement, then 1 mg every 2 months when the underlying cause is irreversible.Obtain diagnostic samples first only when this causes no delay. Hypersensitivity is uncommon but possible; acneiform eruptions and injection-site reactions occur, and serum B12 after treatment should not guide neurological recovery.
Hydroxocobalamin without neurological involvementGive 1 mg intramuscularly three times a week for 2 weeks, then 1 mg every 2 to 3 months when ongoing maintenance is required.Confirm cause and whether maintenance is lifelong. A brisk marrow response can expose iron or folate deficiency, and rare hypokalaemia has been described during severe haematological recovery.